Changes that occur within the cardiac cell in response to Beta-adrenergic stimulation result in a dual effect on the mammalian cardiac contraction: a potentiating effect, manifest as an enhancement of twitch force, and a relaxant effect, evidenced by a decrease in the time to peak force and twitch duration, an enhanced rate of relaxation. Although the relaxant effects can occur in the absence of twitch potentiation, it is not known whether the cellular events that result in the relaxant effect are a prerequisite for twitch potentiation in mammalian cardiac muscle. One approach toward an understanding of this would be to selectively block the relaxant effect of Beta-adrenergic stimulation. We and others have demonstrated a reduction in the cAMP-dependent protein kinase-mediated stimulation of the rate of calcium accumulation in sarcoplasmic reticulum isolated from the hyperthroid heart compared to euthyroid controls. In as much as increased rate of calcium accumulation by SR is a potential mechanism for the cAMP-mediated relaxant effect, these findings suggested to us that the hyperthyroid heart may provide a useful model in which the twitch potentiation and changes in transmembrane ionic flux in response to Beta-adrenergic stimulation might be dissociated from the usually concomitant relaxant effect.